| Project/Area Number |
18K07177
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 49070:Immunology-related
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| Research Institution | Osaka University |
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Principal Investigator |
Ichiyama Kenji 大阪大学, 免疫学フロンティア研究センター, 特任准教授(常勤) (60777960)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2019: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 制御性T細胞 / 長鎖非翻訳RNA / Foxp3 / 自己免疫疾患 / CRISPRi / エピジェネティクス |
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| Outline of Final Research Achievements |
In order to establish the molecular basis of Treg differentiation via the transcription factor Satb1, we focused on the role of Ikzf1, which a transcription factor that forms a complex with Satb1, in Treg. Then, the loss of Ikzf1 function in Treg causes abnormal activation of immune responses and the development of autoimmune disease-like lethal inflammation, suggesting that Ikzf1 plays an important role in Treg.
At the same time, we also conducted a large-scale screening using own CRISPRi system to identify novel LncRNAs involved in Treg differentiation, and succeeded in identifying many novel LncRNAs as candidates for regulators of Treg differentiation.
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| Academic Significance and Societal Importance of the Research Achievements |
正常個体中に存在する制御性T細胞(Treg)は、異常・過剰な免疫反応の抑制に特化したT細胞群であり、免疫自己寛容、免疫恒常性の維持に中心的な役割を果たしている。そしてその異常は、自己免疫病、アレルギー疾患、炎症性腸炎などの直接的原因となることが知られている。本研究成果は、Tregの分化機構および免疫抑制機構の基礎的理解を進めた。このことから、Tregを標的とし、その量的・機能的増減による、癌、病原微生物や自己免疫疾患、移植臓器拒絶反応に対する新しい免疫応答制御法の開発、医療応用が期待できる。
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